Chapter 06
Diagnostic Reasoning
Pattern recognition with explicit steps. Two tools here: the central-vs-peripheral differentiation framework adapted from McCaslin's Table 5–3, and four worked cases that walk you from history through battery to interpretation.
The distinguishing features below are drawn from McCaslin's clinical synthesis of Leigh & Zee and Baloh.[McCaslin 2013][Leigh & Zee 2006] BPPV management recommendations follow the AAO-HNS clinical practice guideline.[Bhattacharyya et al. 2017]
Feature
Peripheral
Central
Direction of nystagmus
Direction-fixed horizontal, with slight torsional component. Beats in one direction regardless of gaze position.
Direction-changing — may reverse in different gaze positions. May be purely vertical (up- or down-beating) or oblique. Rebound nystagmus possible.
Effect of visual fixation
Suppressed by fixation. Intensity increases when vision is denied (goggles covered) — a hallmark feature.
Not suppressed by fixation. May persist or even intensify with vision. Removing fixation produces little change.
Behaviour with eccentric gaze
Follows Alexander's law: amplitude increases on gaze toward the fast phase, decreases on gaze toward the slow phase.
Does not follow Alexander's law. Amplitude may be equal in all eccentric positions, or change paradoxically.
Oculomotor battery
Saccades, smooth pursuit, OPK — typically all NORMAL.
Often abnormal: dysmetric saccades, saccadic pursuit, asymmetric OPK. Clear localising value.
Caloric response
Often shows unilateral weakness (≥25% by Jongkees) on the affected side.
Usually symmetric. Hyperactive responses or perverted responses (vertical instead of horizontal) suggest central pathology.
Time course
Acute onset, then static & dynamic compensation over weeks. Symptoms wane even when lesion persists.
Variable; depends on aetiology. Compensation often incomplete or absent. Progressive or fluctuating courses common.